Pure lecithin is also referred to as L-.alpha.-lecithin or L-.alpha.-phosphatidylcholine (PC). This compound has the general formula (R.sub.1 CO.sub.2 CH.sub.2 --)R.sub.2 CO.sub.2 CH(--CH.sub.2 OPO.sub.2.sup.- --OCH.sub.2 CH.sub.2 N (CH.sub.3).sub.3.sup.+), wherein the groups R.sub.1 CO.sub.2 -- and R.sub.2 CO.sub.2 -- are derived from one or more fatty acids such as stearic, oleic, palmitic, palmitoleic, linoleic, linoledonic acid and arachidonic acid. Naturally-occurring lecithin, derived from sources such as bovine organs, egg yolk or soybeans, provides most of the choline that is present in the diet, and its consumption raises blood choline levels The average dietary intake of PC has been estimated to be 2.6-5.8 g/day. Therefore, if the average person consumes 8-10 g of pure PC, blood choline levels will about double.
After PC is consumed, half of it is rapidly broken down within the intestines to yield choline, which enters the blood stream. The other half is absorbed into the lymph without being degraded; it aids in metabolizing cholesterol and other fats, and eventually some of its choline content enters the bloodstream.
Choline itself is rarely ingested because most foods contain choline in the form of PC. Administration of choline salts, rather than PC, is an inefficient way to increase blood choline levels because most of the free choline is destroyed by bacteria in the intestines. Furthermore, this bacterial action provides amines, which give the body an unpleasant odor of rotten fish. Therefore, the administration of PC is the preferred way to raise blood choline levels. Choline circulating in the blood after PC ingestion is taken up into all cells of the body. The brain has a unique way of ensuring that its nerve cells will receive adequate supplies of circulating choline. A protein molecule within the brain's capillaries traps the circulating choline, and then transports it across the blood-brain barrier, into the brain. Once in the brain, choline is incorporated into the brain's own PC, which is an essential and major part of neuronal membranes. See J. K. Blusztajn et al., Science, 221, 614 (1983). Circulating choline transported into the brain has an additional function for a special group of nerve cells that make acetylcholine, which is released into synapses as a neurotransmitter. The choline provides the essential precursor used to synthesize acetylcholine (R. J. Wurtman et al., in Alzheimer's Disease: A Report of Progress in Research, S. Corkin et al., eds., Raven Press, NY (1982)). In the absence of adequate choline, the ability of these nerve cells to transmit messages to other cells across synapses is impaired. In contrast, when supplemental choline is provided, these messages can be amplified. These findings, based upon studies in experimental animals, isolated organs, and cultured cells, provide the scientific basis for using PC supplements to increase acetylcholine release, especially in clinical conditions and disorders where cholinergic tone is impaired (R. J. Wurtman et al., Pharma-col. Rev., 32, 315 (1981)). Thus, PC's ability to increase blood choline, brain choline, and brain acetylcholine levels has led to its use as a supplement for patients with brain diseases associated with impaired acetylcholine neurotransmission, such as tardive dyskinesia (TD). Similarly, PC's central role in the composition and functional properties of neuronal membranes suggests its utility as a supplement for patients with brain diseases associated with the dissolution of neuronal membranes, such as Alzheimer's disease. The utility of PC (and choline) as a nutritional supplement is best documented in TD, although it has been tested in patients with a variety of brain diseases, including Alzheimer's disease, Huntington's disease, Gilles de la Tourette syndrome, familial ataxia, myasthenia gravis, epilepsy, and mania. J. H. Growdin et al. (U.S. Pat. No. 4,221,784) disclose the use of lecithin to alleviate the effects of TD, manic-depressive disease, memory impairment and familial ataxia I. V. Jackson et al., in Am. J. Psychiatry, 136, 11 (1979) reported a significant improvement in six patients with moderate or severe TD who were given 50 g/day of lecithin for two weeks. A. Little et al., J. Neurology, 48, 736 (1985) reported that administration of 20-25 g of purified soya lecithin to Alzheimer's disease patients for six months improved the performance in an older subgroup of patients who had been identified as "poor compliers."
In order for olfaction (the sense of smell) to occur, the odoriferous chemicals must move through the nose to the olfactory receptors and then through the olfactory nerve to the olfactory bulb. The signal of the smell then progresses through the olfactory bulb to the brain. Acetylcholine is present in the olfactory bulb, and nasal administration of acetylcholine has been reported to lead to increased olfactory acuity. Furthermore, the anesthetic scopolamine lowers acetylcholine levels and has been reported to decrease olfactory detection in normal subjects. More than 200,000 patient visits to physicians occur each year because of complaints relating to smell and/or taste. Approximately four million Americans have abnormalities in their ability to smell or taste, and more than 90% of these patients have abnormalities in the sense of smell.
Therefore, a need exists for a method to reverse hyposmia (decreased sense of taste and smell) or anosmia (absence of sense of taste and smell), without deleterious side effects.